Transverse myelitis after SARS‐CoV‐2 infection: Report of two cases with COVID‐19

Advani, Soroor; Hosseini, Seyyed Mohammad‐Mahdi; Zali, Alireza; Ommi, Davood; Fatemi, Alireza; Khoshnoud, Reza Jalili; Ashrafi, Farzad

doi:10.1002/ccr3.5196

Cited by 9 publications

(8 citation statements)

References 25 publications

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“…Two potential proposed theories describe how SARS-CoV-2 may cause neurological complications such as Transverse Myelitis. The rst being through direct neuroinvasion in which SARS-CoV-2 infects the brain and spinal cord through its binding receptor, angiotensin-converting enzyme 2, ACE2 [3]. ACE2 receptors are most abundantly found in the lung cells leading to the upper respiratory manifestations most often seen in COVID-19 positive individuals.…”

Section: Discussionmentioning

confidence: 99%

“…While there is no single etiology of transverse myelitis, there have been numerous proposed etiologies, including paraneoplastic, autoimmune (perhaps due to multiple sclerosis or acute disseminating encephalomyelitis), and para-infectious causes (due to Herpes simplex virus or Mycoplasma pneumoniae) in which the body's response to the foreign pathogen mistakenly affects proteins in myelin. There have been few cases published regarding TM and COVID-19 as the complication is quite rare [3,4,5,6]. Here we present the case of a healthy, immuno-competent woman who developed a case of transverse myelitis after previously being infected with the COVID-19 virus.…”

Section: Introductionmentioning

confidence: 93%

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A Case of Transverse Myelitis Secondary to COVID-19 Infection

Borra

Patel

Shaikh

et al. 2022

Preprint

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Infection with COVID-19 (SARS-CoV-2) is associated with a variety of generalized and specific symptoms, including neurological complications of both the peripheral and central nervous system. In this case report, we present the case of a previously healthy 55-year-old woman who was diagnosed with transverse myelitis following a previous infection with COVID-19. Her initial presenting symptoms were numbness and tingling of the abdomen, neurogenic bladder, hyperreflexia of the bilateral lower extremities, positive Babinski sign, sensory decrement to pin prick below T5 dermatome, and generalized weakness over the previous 20 days with slow progression caudally into the bilateral lower extremities that resulted in difficulties ambulating. She had no symptoms of the upper extremities or face and denied ever previously experiencing similar symptoms. MRI showed progressive demyelination of the cervical, and thoracic spinal cord, cerebrospinal fluid (CSF) showed increased levels of protein and red blood cells and no markers of infection, including negative PCR for COVID-19 antibodies. The patient was treated with a course of methylprednisolone, multiple treatments of plasmapheresis, and ongoing treatment with rituximab, all of which were well-tolerated. She was instructed to follow-up with her primary care physician 5–7 days after hospital discharge.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 93%

A Case of Transverse Myelitis Secondary to COVID-19 Infection

Borra

Patel

Shaikh

et al. 2022

Preprint

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“…39 Case reports and review articles have reported COVIDÀ19-associated transverse myelitis with onset 7 to 21 days following COVIDÀ19 symptoms or diagnosis. [40][41][42] Nine out of 10 patients from these reports had spinal cord lesions that extended along three or more vertebrae without abnormal brain MRI findings (►Fig. 4).…”

Section: Transverse Myelitismentioning

confidence: 99%

“…4). [40][41][42] One patient had severe diffuse weakness and paraplegia with an extensive spinal cord lesion and without evidence of ADEM on brain MRI. 41 Given the postinfectious delay between infection and symptom onset, it has been suggested that COVIDÀ19-associated transverse myelitis is immune-mediated, possibly with pathophysiology similar to ADEM.…”

Section: Transverse Myelitismentioning

confidence: 99%

Neuroimaging of COVID-19

Kim

Young

2023

Semin Neurol

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We review the wide variety of common neuroimaging manifestations related to coronavirus disease 2019 (COVID-19) and COVID therapies, grouping the entities by likely pathophysiology, recognizing that the etiology of many entities remains uncertain. Direct viral invasion likely contributes to olfactory bulb abnormalities. COVID meningoencephalitis may represent direct viral infection and/or autoimmune inflammation. Para-infectious inflammation and inflammatory demyelination at the time of infection are likely primary contributors to acute necrotizing encephalopathy, cytotoxic lesion of the corpus callosum, and diffuse white matter abnormality. Later postinfectious inflammation and demyelination may manifest as acute demyelinating encephalomyelitis, Guillain–Barré syndrome, or transverse myelitis. The hallmark vascular inflammation and coagulopathy of COVID-19 may produce acute ischemic infarction, microinfarction contributing to white matter abnormality, space-occupying hemorrhage or microhemorrhage, venous thrombosis, and posterior reversible encephalopathy syndrome. Adverse effects of therapies including zinc, chloroquine/hydroxychloroquine, antivirals, and vaccines, and current evidence regarding “long COVID” is briefly reviewed. Finally, we present a case of bacterial and fungal superinfection related to immune dysregulation from COVID.

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“…There are numerous proposed etiologies for TM, including paraneoplastic, autoimmune (perhaps due to multiple sclerosis or acute disseminating encephalomyelitis), and para-infectious causes (due to Herpes simplex virus or Mycoplasma pneumoniae) in which the body's response to the foreign pathogen mistakenly affects proteins in myelin. A few cases have been published regarding TM and COVID-19 as the complication is quite rare [ 5 - 10 ]. Here, we present the case of a healthy, immunocompetent woman who developed a case of TM after being infected with the COVID-19 virus.…”

Section: Introductionmentioning

confidence: 99%